Klebsiella pneumoniae als mogelijke oorzaak van hypertensie
Translationele studie suggereerde een causale relatie tussen de darmpathogeen Klebsiella pneumoniae en hypertensie. Het microbioom-concept in hypertensie breidt zich uit, maar de klinische relevantie vereist bevestiging in interventionele studies.
Abstract (original)
BACKGROUND: Previous studies have reported a strong association between gut microbiome and hypertension; yet, the exact bacterial species associated with the disease development and progression have not yet been detected. This study aimed to investigate whether opportunistic pathogen Klebsiella pneumoniae is a causal factor for hypertension pathogenesis, and explore the potential mechanisms. METHODS: The enrichment of Klebsiella pneumoniae in the gut of patients with hypertension was validated by meta-analysis based on 3 independent cohorts. Klebsiella pneumoniae was inoculated into germ-free mice, antibiotic pretreated and conventional mice. RESULTS: Klebsiella pneumoniae led to higher blood pressure, slight cardiac hypertrophy, and enhanced contractility of resistant arteries in recipient mice. Moreover, Klebsiella pneumoniae induced pathological damages, deficiency of tight junction proteins and transcriptional shifts. Metabolic alterations, especially the depletion of stearoylethanolamide, were observed upon Klebsiella pneumoniae administration. In addition, renal transcriptome dysfunction with significant upregulation of genes related to hypertension pathogenesis was observed in Klebsiella pneumoniae treated mice. CONCLUSIONS: These results provide evidence that the enrichment of Klebsiella pneumoniae acts as a direct contributor to blood pressure elevation and hypertension pathogenesis, and Klebsiella pneumoniae induced intestinal damages, fecal metabolic changes, and renal shifts may be integrated mediators.
Dit artikel is een samenvatting van een publicatie in Hypertension (Dallas, Tex. : 1979). Voor het volledige artikel, alle details en referenties verwijzen wij u naar de oorspronkelijke bron.
Lees het volledige artikelDOI: 10.1161/HYPERTENSIONAHA.122.18878